Drag-reducing polymers were discovered by B. A. Toms in 1949.1 They are successfully used to increase the speed and reduce the noise of ships, submarines, and torpedoes; to reduce the pumping costs of liquids; to reduce energy losses in two-phase flow; and to increase the throw of sprinkler systems and firefighting equipment.
Drag-reducing polymers (DRP) are long (MW>106), soluble, linear polymers, with axial elasticity. Polyethylene oxide (PEO) and polyacrylamide are prototypical examples. Addition of 2 to 100 ppm of these polymers will reduce the pressure drop of fluid flowing in a pipe by up to 70% and decrease the drag on a ship's hull by up to 80%.2 
The mechanism(s) of action of DRP are still not understood completely. It has become clear that the axial elasticity of the molecules are vital to their function.3 The molecules appear to act as shock absorbers, damping out turbulent eddies. It has also been shown that DRP inhibit the shedding of laminar boundary layer flow into the turbulent flow near surfaces. At the low concentrations where DRP are typically used, they have no effect on the fluid viscosity. Furthermore, the drag-reducing effects of DRP are seen in turbulent flow, but not in laminar flow.
Since blood flow is laminar throughout the body, scientists were surprised to find measurable effects of DRP when added to blood. Subsequent work indicates that DRP reduce flow disturbances at bifurcations such as branches in capillary networks and reduce the thickness of the cell free layer near vessel walls.4-6 
Reports of beneficial effects of DRP in animals started appearing during the 1970's. Mostardi, et al. showed that polyacrylamide reduced the frequency of flow separation from the aortic wall below a stenosis by 60%.7 In 1987, Coleman et al. published that polyacrylamide increased cardiac output more than two-fold and reduced peripheral resistance by half.8 Two years later, they showed that polyethylene oxide increased aortic blood flow, reduced heart rate, increased ventricular and arterial blood pressure, and reduced peripheral resistance.9 The next year, Ertepinar, et al. showed that chronic infusion of polyacrylamide into guinea pigs significantly reduced the formation of atherosclerotic plaques.10 
Marina Kameneva kept interest in DRP alive over the subsequent decades. She began working in the field in Russia during the 1980's and brought her interest to the US during the 1990's. In 2004, she published work showing that a high MW PEO and an extract from aloe vera each protects rats from hemorrhagic shock, while rats receiving low MW PEO or saline showed poor tissue perfusion and 80-85% mortality rates. Two years later, she demonstrated that high MW PEO dramatically increased perfusion in dog hearts following stenosis of the left anterior descending coronary artery.12 In 2007, she published data showing that the DRP from aloe vera protected rats from a severe AMI, while 50% of the control animals died.13 
Acute Renal Failure
Acute renal failure (ARF) is the sudden loss of the kidney's ability to filter wastes without losing electrolytes. Most often, ARF (also termed acute kidney injury or AKI) is caused by reduced blood flow to the kidneys (prerenal ARF), though about 20% of the cases are due to infections or toxins affecting the kidneys directly (intrinsic ARF), and about 10% are due to blockages downstream of the kidneys (postrenal obstruction).
The incidence of community acquired ARF is only about 100 cases per million population with a mortality rate of 7%.14 The published incidence of ARF ranges from 1 to 13% of all hospital admissions (34×106/year in the US) and 20 to 30% of all ICU admissions (4.4×106/year in the US).15 Most cases of ARF are acquired in the hospital as a result of complications from other illnesses or interventions. The most common causes are sepsis, hypovolemia, surgery, imaging contrast agents, chemotherapy drugs, NSAIDS, and some antibiotics.
There has been only one study of the incidence of ARF at the national level. Using the 2001 National Hospital Discharge Survey Liangos, et al, found that 1.9% of all hospital discharges showed a code for ARF, which corresponds to a U.S. incidence of 646,000. The mortality rate was 21.3%. The authors validated the study by examining all the 13,237 patients discharged from St. Elizabeth's (Boston) during 2001. 2.6% of the patients were coded for ARF, but lab values showed that 12% of the patients had experienced ARF. Thus, ARF is coded on only about 20% of occurrences (presumably the most serious cases).16 
The treatment of ARF is to give fluids to reverse hypovolemia and flush toxins while waiting for the kidneys to recover. In some instances, the patients retain too much water or their electrolyte balance suffers to such an extent that they require dialysis. The most common causes of death in ARF patients are heart failure, sepsis, and respiratory failure. Patients who recover from ARF show increased odds of death and chronic kidney disease over the following 5 and 10 years. Dozens of new treatments and drugs that showed promise in animals have been tested clinically in ARF patients, but none have demonstrated benefits in randomized clinical trials. Some of the treatments tested include diuretics to increase urine flow, dopamine and atrial natriuretic peptide (ANP) to increase blood flow to the kidneys, many cytoprotective agents to preserve tubule epithelial cells such as free radical scavengers, heat shock proteins, hemeoxygenase, xanthine oxidase inhibitors, prostaglandins, and calcium channel blockers and, recently, several growth factors to speed the recovery of the proximal tubules.′5 
No one has recognized that the properties of DRP would make them useful in patients suffering renal failure. Two groups looked at the effects of DRP on kidneys 20 years ago and found they are effective as diuretics. In 1987, Smyth, et al. published that a polyacrylamide DRP in rats increased urine and sodium excretion without altering potassium excretion or creatinine clearance.17 Three years later, they published results using both a PEO and a polyacrylamide in rats showing that each DRP increased diuresis and natriuresis without altering creatinine clearance or potassium excretion.18 In 1987, Sumpio, et al. tested polyacrylamide buffer solutions containing 10 and 20% RBC's in perfused kidneys. They found a strong interaction between the effects of hematocrit and the DRP on kidney function. For example, the GFR was reduced by the DRP at 10% Hct but increased at 20% Hct.19 Presumably, interest waned in DRP as an injectable diuretic with the advent of many orally active diuretics. It is important to note that diuresis is contraindicated in patients experiencing ARF. No other work using DRP in the renal field has been published since.
Thus, I was surprised to find such a dramatic benefit of DRP in the treatment of ARF. ARF has been a serious health problem which has not seen any new, successful treatments since dialysis was introduced in the 1970's. It is unfortunate that no one has thought to study DRP as a treatment for ARF until now.